IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Joyce, E. A.
Right arrow Articles by Wright, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Joyce, E. A.
Right arrow Articles by Wright, A.

 Previous Article  |  Next Article 

Infection and Immunity, July 2001, p. 4202-4209, Vol. 69, No. 7
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.7.4202-4209.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Differential Gene Expression from Two Transcriptional Units in the cag Pathogenicity Island of Helicobacter pylori

Elizabeth A. Joyce,1,dagger Joanne V. Gilbert,2 Kathryn A. Eaton,3 Andrew Plaut,2 and Andrew Wright1,*

Department of Microbiology and Molecular Biology, Tufts University School of Medicine,1 and Division of Gastroenterology, Department of Medicine, New England Medical Center,2 Boston, Massachusetts 02111, and Department of Veterinary Biosciences, Ohio State University, Columbus, Ohio 432103

Received 11 January 2001/Returned for modification 20 February 2001/Accepted 3 April 2001

Infection with Helicobacter pylori strains containing the cag Pathogenicity Island (cag PAI) is strongly correlated with the development of severe gastric disease, including gastric and duodenal ulceration, mucosa-associated lymphoid tissue lymphoma, and gastric carcinoma. Although in vitro studies have demonstrated that the expression of genes within the cag PAI leads to the activation of a strong host inflammatory response, the functions of most cag gene products and how they work in concert to promote an immunological response are unknown. We developed a transcriptional reporter that utilizes urease activity and in which nine putative regulatory sequences from the cag PAI were fused to the H. pylori ureB gene. These fusions were introduced in single copies onto the H. pylori chromosome without disruption of the cag PAI. Our analysis indicated that while each regulatory region confers a reproducible amount of promoter activity under laboratory conditions, they differ widely in levels of expression. Transcription initiating upstream of cag15 and upstream of cag21 is induced when the respective fusion strains are cocultured with an epithelial cell monolayer. Results of mouse colonization experiments with an H. pylori strain carrying the cag15-ureB fusion suggested that this putative regulatory region appears to be induced in vivo, demonstrating the importance of the urease reporter as a significant development toward identifying in vivo-induced gene expression in H. pylori.

* Corresponding author. Mailing address: Department of Microbiology and Molecular Biology, Tufts University School of Medicine, 136 Harrison Ave., Boston, MA 02111. Phone: (617) 636-6758. Fax: (617) 636-3307. E-mail: andrew.wright{at}tufts.edu.

dagger Present address: Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305.

Infection and Immunity, July 2001, p. 4202-4209, Vol. 69, No. 7
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.7.4202-4209.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2001 by the American Society for Microbiology. All rights reserved.